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Volume 64 (1994)
- Issue 4 Pages 229-
- Issue 3 Pages 135-
- Issue 2 Pages 65-
- Issue 1 Pages 1-
Volume 64, Issue 2
Displaying 1-10 of 10 articles from this issue
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Ikuko Kimura, Yukiko Hata, Md. Amirul Islam, Masayasu Kimura1994 Volume 64 Issue 2 Pages 65-70
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe mechanisms responsible for diabetes mellitus-induced enhancement of prostaglandin (PG) F2α response were investigated in vascular smooth muscles isolated from diabetic mice and rats. Streptozocin (150 mg/kg, i.v. bolus, 6 week-elapsed)-ddY mice and (60 mg/kg, i.v. bolus)-Wistar rats and genetically diabetic GK-rats were used. The responses to PGF2α were enhanced in small blood vessels such as mesenteric arteries (diabetic rats) and veins (diabetic mice) and they were reduced in large blood vessels such as the aorta and vena cava (diabetic rats). The enhanced response to PGF2α in diabetic blood vessels was significantly inhibited by nordihydroguaiaretic acid (NDGA) (0.03 mM) and phenidone (0.05 mM), lipoxygenase inhibitors, cycloheximide (1 mg/kg, i.v.), a protein synthesis inhibitor and actinomycin D (2.8 mg/kg, i.v.), a RNA polymerase inhibitor, but neither inhibited by cyclooxygenase inhibitors, a thromboxane antagonist, nor Ca2+ antagonists. The PGF2α response was also enhanced with aging alone, whereas the extent of enhancement was less than that with diabetes mellitus, and not significantly blocked by NDGA. These results demonstrate that diabetes mellitus-induced imbalance in the regulation of the eicosanoid metabolic pathways (suppressed cyclooxygenase and accelerated lipoxygenase) may cause the enhancement of PGF2α-induced responses in small blood vessels.View full abstractDownload PDF (381K) -
Fusako Takayama, Toru Egashira, Yasumitsu Yamanaka1994 Volume 64 Issue 2 Pages 71-78
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe present study investigated the effects of diclofenac sodium (Dic Na) on lipid peroxidation (LPO) and liver injury in ischemia-reperfused rats. LPO was estimated from the levels of phosphatidylcholine hydroperoxide (PCOOH), a primary peroxidative product of phosphatidylcholine. Hepatic ischemia-reperfusion induced significant elevation of plasma PCOOH and caused liver injury in rats. Rats were treated daily with Dic Na or α-tocopherol (α-toc.), p.o., for 5 days and once at 1 hr prior to induction of ischemia. Both substances prevented LPO from decreasing the plasma PCOOH level, and they significantly suppressed the elevation of serum GOT and LDH, in a dose-dependent manner. Dic Na was able to scavenge the stable free radical 1, 1-diphenyl-2-picrylhydrazyl (DPPH), but did not show radical-trapping ability for superoxide anion (O2-) or hydroxyl radicals (·OH), nor a suppressive ability for the NADPH-dependent LPO of microsomes. In contrast, α-toc. trapped both DPPH and O2-, but not ·OH, and it inhibited the NADPH dependent LPO in vitro. These results suggest that Dic Na may suppress liver injury caused by ischemia-reperfusion through stable radical scavenging and the inhibition of superoxide production in activated phagocytes, both of which may restrain the induction and progression of oxidative stress.View full abstractDownload PDF (549K) -
Hajime Taniguchi, Tadashi Nagamatsu, Ryoji Kojima, Mikio Ito, Yoshio S ...1994 Volume 64 Issue 2 Pages 79-88
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSABSTRACT-To establish the regimen for beneficial prolonged treatment with glucocorticoids on nephritis, we investigated the antinephritic effect of methylprednisolone suleptanate (MPS) and its influence on adrenal function by intermittent administration (IA) in comparison with daily administration (DA) in crescentic-type anti-GBM nephritic rats. In IA, MPS (0.25, 1.0 and 3.0 mg/kg) was injected for 3 successive days followed by a 3-day withdrawal during a 40-day period. MPS inhibited the elevation of urinary protein and serum cholesterol and glomerular alterations by both IA and DA. The effect of MPS on these parameters was more potent by IA than by DA. MPS significantly suppressed the increment of the number of ED-1(+) cells and TH-1(+) cells in nephritic glomeruli. DA, but not IA, caused atrophy of the adrenal glands. IA prevented the remarkable decrease in corticosterone level provoked in nephritic rats. In conclusion, for the treatment of nephritis, IA seems to be a better regimen for the administration of MPS. MPS may exert an antinephritic action by inhibiting mesangial cell proliferation and infiltration of monocytes/macrophages into glomeruli in addition inhibiting antibody production.View full abstractDownload PDF (1163K) -
Kiyokazu Naganobu, Katsuaki Ito1994 Volume 64 Issue 2 Pages 89-96
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSWe investigated the role of the sarcoplasmic reticulum (SR) in the regulation of cytoplasmic Ca2+ ([Ca2+]i) during α1-adrenoceptor-mediated contraction in rat mesenteric resistance arteries. Phenylephrine (PE) at 1 μM elevated the tension and [Ca2+]i measured with fura-2 in Ca2+-containing PSS, but did not do so in Ca2+-free PSS, suggesting that the contraction elicited by this concentration depends on the Ca2+ influx. Caffeine (100 mM) was shown to discharge Ca2+ in the SR, and cyclopiazonic acid (CPA, 10 μM) was shown to inhibit the Ca2+ uptake into the SR in these arteries. In resting arteries, both CPA and ryanodine (10 μM) sustainedly elevated [Ca2+]i without affecting the tension. In PE-stimulated arteries, both agents caused transient increase in [Ca2+]i, which was larger than that in resting arteries, and augmented the contraction. In the presence of PE, the caffeine-evoked [Ca2+]i transient was more greatly decreased after the application of ryanodine than after CPA. The CPA-induced rise in [Ca2+]i could be ascribed to inhibition of Ca2+ buffering by the SR, and the ryanodine-induced one can be attributed to the acceleration of Ca2+ release. It is suggested that both Ca2+ release from and Ca2+ uptake into the SR are enhanced during PE-induced contraction, which depends on the transmembrane Ca2+ influx.View full abstractDownload PDF (506K) -
Kuniaki Suzuki, Yoshitaka Yoshimura, Yoh Hisada, Akira Matsumoto1994 Volume 64 Issue 2 Pages 97-102
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe inhibitory effect of levamisole and L-homoarginine on alkaline phosphatases (ALP, orthophosphoric monoester phosphohydrolase, EC. 3. 1. 3. 1) in various tissues was studied to characterize differences in the mechanism of inhibition of ALP isoenzymes. The ALP activity from the placenta, kidneys, and a clonal osteogenic cell line, MC3T3-E1, was hyperbolically inhibited with a dependency on the concentration of levamisole (Ki0.5=10-12 μM) or L-homoarginine (Ki0.5=1 μM), but the activity of in testinal ALP was little inhibited by 240 μM levamisole and sigmoidally inhibited by L-homoarginine (Ki0.5 =13 mM) . Hill plot analysis of the L-homoarginine inhibition data showed that the Hill coefficient values of the placenta, kidney, and osteogenic cells were around 0.9-1.0 and that of the intestine was 1.8. The effect of sodium dodecyl sulfate (SDS), which may decrease the subunit-subunit interaction, on the L-homoarginine inhibition of the intestinal ALP was tested. The L-homoarginine concentration-dependent inhibition curve changed from sigmoidal to hyperbolic, and the Hill coefficients decreased with increasing concentrations of SDS. These results suggest that the differences in inhibition by L-homoarginine and affinity changes of intestinal ALP for L-homoarginine are caused by the subunit-subunit interaction of oligomers.View full abstractDownload PDF (403K) -
Ikuko Kimura, Noboru Nakashima, Tokie Komori, Yukihiko Kameda, Masayas ...1994 Volume 64 Issue 2 Pages 103-107
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe glucose-dependency of cholecystokinin-8 (CCK-8)-stimulated insulin release was investigated at high (11.1 and 16.7 mM) glucose concentrations in rat pancreas perfusion and islet perifusion using glucose analogues, pseudo-α-D-glucose and 2-deoxy-D-glucose. In perfused pancreas, both glucose analogues (22.4 mM) inhibited high glucose (16.7 mM)-induced insulin release, but not normal glucose (5.6 mM)-induced insulin release, with or without CCK-8 (1 nM). In perifused islets, the same level of either of the glucose analogues inhibited high glucose (11.1 mM)-induced insulin release, with or without CCK-8 (100 nM). These results demonstrate that CCK-8-stimulated insulin release only at high glucose level is glucose-dependent.View full abstractDownload PDF (348K) -
Fumihiko Okada, Yoshifumi Torii, Hiroshi Saito, Norio Matsuki1994 Volume 64 Issue 2 Pages 109-114
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe antiemetic effects of six serotonergic 5-HT1A-receptor agonists, 8-hydroxy-2-(di-n-propylamino)tetrarin (8-OH-DPAT), 4-{4-[4-(2-pyrimidinyl)piperazin-l-yl]butyl}-2, 3, 4, 5-tetrahydro-l, 4-benzo-xazepine-3, 5-dione (SUN8399), buspirone, gepirone, ipsapirone and tandospirone, against motion sickness were investigated in Suncus murinus. Subcutaneous injection of all six agonists completely and dose-dependently suppressed motion-induced emesis. Pretreatment with 8-OH-DPAT or SUN8399 dose-dependently inhibited emesis elicited by nicotine (4.0 mg/kg, s.c.), veratrine (0.7 mg/kg, s.c.), cisplatin (20 mg/kg, i.p.) and copper sulfate (40 mg/kg, p.o.). These results suggest that serotonergic 5-HT1A-receptor agonists are effective as anti-motion sickness drugs, and these drugs may block a common mechanism(s) for the emetic reflex of the suncus because the antiemetic effects of the 5-HT1A-receptor agonists were exerted irrespective of the stimulus.View full abstractDownload PDF (322K) -
Tetsuo Matsui, Yoshiyuki Nakamura, Hiromichi Ishikawa, Akihiro Matsuur ...1994 Volume 64 Issue 2 Pages 115-124
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSSPR-210 {2-[4-(4, 5, 7-trifluorobenzothiazol-2-yl)methyl-3-oxo-3, 4-dihydro-2H-1, 4-benzo-thiazin-2-yl] acetic acid}, a novel aldose reductase (AR) inhibitor, exhibited highly potent inhibition of partially purified AR from porcine lens (IC50=9.5×10-9 M) and human placenta (IC50=1.0×10-8M). On the other hand, very weak inhibition by SPR-210 was observed against human placenta aldehyde reductase, which is the most closely related enzyme to AR, and against several adeninenucleotide-requiring enzymes. SPR-210 showed a noncompetitive mechanism with respect to DL-glyceraldehyde against porcine lens AR. Sorbitol accumulation in isolated human erythrocytes was effectively inhibited by SPR-210 during incubation with 50 mM glucose (IC50=1.6×10-8M). Oral administration of SPR-210 (1-30 mg/kg/day for 5 days) to streptozotocin-induced diabetic rats decreased the sorbitol contents in the sciatic nerve and lens (ED50=1.9 and 6.8 mg/kg/day, respectively). SPR-210 had higher potency in the lens than other AR inhibitors. Moreover, the deterioration in motor nerve conduction velocity in diabetic rats was ameliorated by treatment with SPR-210 (1-30mg/kg/day) accompanying the reduction in sorbitol content in the sciatic nerve. SPR-210 induced the recovery of the delayed peak latency of oscillatory potentials (O1 O4) in the electroretinogram in diabetic rats (10 mg/kg/day). These results suggest that the specific AR inhibitor SPR-210 will be a useful therapeutic agent for preventing and improving some diabetic complications, especially diabetic neuropathy and retinopathy, and therefore, can be discriminated from other AR inhibitors.View full abstractDownload PDF (646K) -
Seitaro Ohkuma, Shi-Hu Chen, Masashi Katsura, Da-Zhi Chen, Kinya Kuriy ...1994 Volume 64 Issue 2 Pages 125-128
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe effect of muscimol on N-methyl-D-aspartate (NMDA)-induced injury of primary cultured cerebral cortical neurons was examined. NMDA induced a dose-dependent leakage of LDH activity, which was significantly inhibited by (±)-5-methyl-10, 11-dihydro-5H-dibenzo-[a, d]cyclopentan-5, 10-imine (MK-801). Muscimol significantly reduced the NMDA-induced increase of lactic dehydrogenase (LDH) leakage, and bicuculline abolished this protective effect of muscimol. Similarly, muscimol reduced the NMDA-induced increase in trypan blue staining of the cells, and bicuculline suppressed this inhibitory action of muscimol. These results suggest that GABAA-receptor stimulation exerts a protective action against the neuronal injury induced by NMDA-receptor activation.View full abstractDownload PDF (381K) -
Noriko Ogiku, Hiroshi Sumikawa, Tomonari Nishimura, Hiroshi Narita, Ry ...1994 Volume 64 Issue 2 Pages 129-133
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSFor this study, we used (NZW × BXSB)F1 male mice as a model of myocardial infarction. The animals were kept on water containing imidapril or enalapril at 60 mg/kg/day from 10 to 27 weeks of age. Imidapril and enalapril significantly reduced the blood pressure. Imidapril reduced the mortality rate more significantly than enalapril did. In the second experiment where imidapril, enalapril and captopril were administered to the mice at 5 mg/kg/day, p.o., both imidapril and captopril significantly reduced the mortality, but enalapril did not. Blood pressure was slightly reduced by these ACE inhibitors. These data suggest that imidapril and captopril are efficacious for the treatment of myocardial infarction and blood pressure reduction hardly contributes to its mechanism of action.View full abstractDownload PDF (338K)
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